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Increased platelet CD36 constitutes a common marker in myeloproliferative disorders
Author(s) -
Thibert V.,
Bellucci S.,
Cristofari M.,
Gluckman E.,
Legrand C.
Publication year - 1995
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1995.tb05357.x
Subject(s) - myeloproliferative disorders , platelet , medicine , cd36 , immunology , pathology , receptor
Summary. The distribution of the major platelet membrane glycoproteins (GP), Ib, IX, IIb‐IIIa and IV (or CD36), which play important roles as receptors for adhesive molecules in haemostasis and thrombosis, was studied in 34 patients with myeloproliferative disorders (MPD): 13 had essential thrombocythaemia (ET), 12 had polycythaemia vera (PV) and nine had chronic myelogenous leukaemia (CML). Only occasionally were modifications of the numbers of GPIb or GPIIb‐IIIa measured using the binding of specific radiolabeled antibodies to platelets. In contrast, 2‐3‐fold increases of the total CD36 content and the surface CD36 expression were measured in almost all patients studied, using a radioimmunoassay and the direct binding of the radiolabelled antibody, FA6‐152, to the platelet surface, respectively. These results indicate that the abnormality affected both the external and internal CD36 pools. Therefore platelet CD36 may be a useful tool for the diagnosis and the follow‐up of MPD patients. Surface CD36 has been proposed as a platelet receptor for thrombospondin, an adhesive glycoprotein that is released from platelets upon activation and promotes aggregate formation. Despite a 2‐fold increase of CD36 molecules, resting and thrombin‐activated platelets from ET patients expressed the same amount of thrombospondin as normal platelets, suggesting that there is not a direct correlation between the CD36 expression and thrombospondin binding either spontaneously or after activation.